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Cerebral vasospasm as a complication of aneurysmal subarachnoid hemorrhage: a brief review

  • Spallone A. 
Reviews

Abstract

Cerebral vasospasm is one of the most dreaded consequences of a ruptured intracranial aneurysm. Although exceptions may be found, the relationship between angiographic narrowing of cerebral arteries and deterioration of clinical status is supported by many authors. The cause of cerebral vasospasm still remains obscure. Several substances such as serotonin, prostaglandins, catecholamines appear to have a vasoconstrictive effect on the cerebral vessels. Recent evidence indicates that erythrocyte lysis within the subarachnoid spaces may play a major role in the genesis of delayed clinically relevant cerebral vasoconstriction following aneurysmal subarachnoid hemorrhage (SAH). The pathophysiology of brain ischemia following aneurysmal rupture, and the correlation between angiographic vasospasm, neurological condition, intracranial pressure (ICP) value, cerebral blood flow and CT findings are briefly discussed. It is concluded that, at present, blood volume expansion and/or induced hypertension, and pharmacological control of increased ICP provide the best basis for clinical management of the cerebral ischemic complications of SAH. Preoperative antifibrinolytic therapy and delayed surgical obliteration of the bleeding aneurysm, i.e. the policy at present most frequently adopted, are currently undergoing critical review in the light of the fact that antifibrinolytic therapy seems to be accompanied by a higher rate of ischemic SAH complications and vasospasm, whilst there are very recent suggestions that the results of early intracranial aneurysm surgery may be better than those of delayed surgery, if account is taken of the patients lost because of recurrent SAH or ischemia during the waiting period.

Key-Words

Intracranial aneurysm subarachnoid hemorrhage cerebral ischemic complications cerebral vasospasm 

Sommario

Il vasospasmo cerebrale è una delle complicanze più terribili della rottura di un aneurisma intracranico. Esiste largo accordo tra gli autori sul fatto che la dimostrazione angiografica di uno spasmo delle arterie cerebrali dopo emorragia subaracnoidea (SAH) è, salvo rare eccezioni, di cattivo significato sul piano clinico-prognostico.

La causa del vasospasmo resta tuttora da chiarire. Varie sostanze, quali serotonina, prostaglandina, norepinefrina, potrebbero avere un ruolo al riguardo. Recentemente ha acquistato sempre maggior credito l'ipotesi che i prodotti della lisi eritrocitaria a livello degli spazi subaracnoidei possono avere un ruolo primario nella genesi del vasospasmo cerebrale.

Vengono considerati gli aspetti fisiopatologici e le correlazioni tra vasospasmo angiografico, condizioni cliniche, pressione intracranica (ICP), flusso cerebrale e tomografia computerizzata (CT).

Dal punto di vista terapeutico, al momento lo schema più idoneo per il trattamento delle complicanze ischemiche dell'emorragia subaracnoidea appare essere rappresentato dall'aumento del volume intravascolare associato o meno a rialzo farmacologico della pressione sistemica.

Il protocollo terapeutico più largamente usato nel trattamento degli aneurismi intracranici-costitutito da uso di farmaci antifibrinolitici in fase acuta ed intervento chirurgico “in fase fredda”-è attualmente in via di riconsiderazione critica. Infatti l'uso degli antifibrinolitici è apparso essere correlato con una maggiore incidenza di vasospasmo e complicanze ischemiche, mentre è stato di recente suggerito che i risultati della chirurgia “precoce”-effettuata cioè entro 3 giorni dall'emorragia-sarebbero superiori a quelli dell'intervento “ritardato”, qualora si tenga conto dei pazienti peggiorati e/o deceduti durante l'attesa.

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© Masson Italia Periodici S.r.l. 1985

Authors and Affiliations

  • Spallone A. 
    • 1
  1. 1.Istituto di Neurochirurgia dell'Università di RomaRoma

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